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KRAS

RNF141 Interacts with KRAS to Promote Colorectal Cancer Progression

[Oncogene] The authors examined the expression of RNF141 in 64 pairs of colorectal cancer and adjacent normal tissues by real-time PCR, Western blot, and immunohistochemical analysis.

Cell Death in Pancreatic Cancer: From Pathogenesis to Therapy

[Nature Reviews Gastroenterology & Hepatology] The authors describe the molecular machinery of cell death, discuss the complexity and multifaceted nature of lethal signalling in pancreatic ductal adenocarcinoma cells, and highlight the challenges and opportunities for activating cell death pathways through precision oncology treatments.

MASTL Regulates EGFR Signaling to Impact Pancreatic Cancer Progression

[Oncogene] Based on a comprehensive investigation involving pancreatic cancer (PC) patient samples, murine models of PC progression, and loss and gain of function studies, researchers reported a previously undescribed critical role of microtubule-associated serine/threonine-protein kinase-like (MASTL) in promoting cancer malignancy and therapy resistance.

MASTL Regulates EGFR Signaling to Impact Pancreatic Cancer Progression

[Oncogene] Based on a comprehensive investigation involving pancreatic cancer (PC) patient samples, murine models of PC progression, and loss and gain of function studies, researchers reported a previously undescribed critical role of microtubule-associated serine/threonine-protein kinase-like (MASTL) in promoting cancer malignancy and therapy resistance.

The Integrated Stress Response Is Tumorigenic and Constitutes a Therapeutic Liability in KRAS-Driven Lung Cancer

[Nature Communications] Researchers demonstrated that integrated stress response was pivotal in lung adenocarcinoma development, the most common histological type of lung cancer and a leading cause of cancer death worldwide.

Mutant Idh2 Cooperates with a NUP98-HOXD13 Fusion to Induce Early Immature Thymocyte Precursor ALL

[Cancer Research] In vitro treatment of Idh2R140Q/NHD13 thymocytes with enasidenib, a selective inhibitor of mutant IDH2, led to a marked decrease in leukemic cell proliferation, demonstrating that Idh2R140Q/NHD13 mice could serve as a useful in vivo model for the study of early/immature T cell precursor acute lymphoid leukemia (ALL) development and therapy.

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